hm....
i was wrong that said fat...
okay.. let said cholesterol plague in that vein....
hm... if i'm not wrong my assistant said that we may find some chlstrl plague... in it..-the vein-
hm... am i wrong when i recalled that memory?
hm...

pocho wrote:what happens to the hepatic portal vein if i have eaten too much meat and what happens to that vein if i have eaten too much bread

Nothing happened as long as your machinery works properly Meat, bread, and other nutrients are processed in the stomach. Only their monomers enter the transportation system. Something bad definetely happened in your stomach, in which you feel "want-to-explode"

The hepatic portal vein (often portal vein for short) is a portal vein in the human body that drains blood from the digestive system and its associated glands. It is one of the main components of the portal venous system.

Hypergalactosaemia and portosystemic encephalopathy could occur due to overeating.

The hepatic portal system begins in the capillaries of the digestive organs and ends in the portal vein. Consequently, portal blood contains substances absorbed by the stomach and intestines. Portal blood is passed through the hepatic lobules where nutrients and toxins are absorbed, excreted or converted.

Restriction of outflow through the hepatic portal system can lead to portal hypertension. Portal hypertension is most often associated with cirrhosis. Patients usually present with splenomegaly, ascites, GI bleeding and/or portal systemic encephalopathy.

The consequences of portal hypertension are due to portal systemic anastomosis formed by the body as an attempt to bypass the obstructed liver circulation. These collateral vessels form along the falciform ligament, diaphragm, spleen, stomach and peritoneum. The collaterals find their way to the renal vein where blood drained from the digestive organs is let into the systemic circulation.

Hypergalactosaemia Reference and Cause:
The clinical presentation and outcome of 15 neonates with porto-systemic (PS) shunt detected by mass screening (Paigen method) for galactosemia are reviewed. Routine screening for galactosemia initially recognized fourteen patients, but one patient was discovered by the presentation of multiple skin hemangiomas and subsequent re-screening for galactosemia. The majority of patients were excluded by enzyme assay for hereditary galactosemias and diagnosed by ultrasonography and /or angiogram as having PS shunts in the neonatal period. Galactose is effectively extracted from portal blood by liver and PS shunts result in hypergalactosemia. The neonates with PS shunts were separated into 3 types. Two patients had congenital absence of portal vein (CAPV) with PS shunt by ductus venosus Arantii. Four had extrahepatic porto-left renal venous (PRV) shunt. Nine neonates presented with intrahepatic porto-hepatic venous (PV) shunts associated with or without multiple hepatic hemangiomas. At diagnosis, galactosemia was present in all patients, but the degree of hypergalactosemia was varied among 3 types (over 16mg/dl in CAPV, 20~6 mg/dl in PV shunts, 10~8 mg/dl in PRV shunt). The bile acids (TBA) are also absorbed by liver and plasma level of total bile acids (TBA) was increased in all patient (297~117 µ M in CAPV, 138~51 µ M in PV shunts, 50~ 46 µ M in PRV shunt). Hepatic hemangiomas regressed in all, but associated PV shunts persisted in 3 cases after 1 to 12 years of follow up. CAPV maintained in nature and PRV shunt was not closed, and hyperammonemia and hypermanganemia presented as late complications for the patients with persistent PS shunts. These results indicate that PS shunt should be suspected in all neonates with increased levels of galactose and TBA, when hereditary galactosemias were excluded. The prognosis varied among 3 types of PS shunts. Careful assessment must be warranted for complications.